medical retina (see DM)

Question 1

5 findings on fundoscopy of non-proliferative retinopathy

Answer 1

1. microaneurysms;
2. exudate;
3. dot haemorrhages;
4. blot haemorrhages;
5. cotton wool spots

Question 2

how does exudate form (diabetic retinopathy)

Answer 2

internal-retinal lipid deposits due to plasma leakage/oedema from microaneurysms or capillaries

Question 3

how do cotton wool spots form (retinopathy)

Answer 3

axoplasmic debris from nerve-fibre infarcts - i.e. debris from death of nerve fibres

Question 4

what is branch retinal vein occlusion

Answer 4

occlusion of a branch of the retinal vein as it is crossed by a retinal arteriole

Question 5

what is central retinal vein occlusion (CRVO)

Answer 5

occlusion of vein in optic nerve as it runs alongside the central retinal artery

Question 6

severe/ischaemic CRVO presentation

Answer 6

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/60-hand motions only at 1m

Question 7

severe CRVO retinal signson fundoscopy (5)

Answer 7

1. severe intraretinal haemorrhages;
2. engorged retinal veins;
3. disc swelling;
4. macular oedema;
5. cotton wool spots

Question 8

what clinical test will be +ve in severe CRVO

Answer 8

RAPD -> indicates severe loss of afferent visual input

Question 9

3 complications of CRVO

Answer 9

rubeotic glaucoma; macular oedema; retinal neovascularisation

all are treatable

Question 10

5 risk factors for CRVO

Answer 10

1. age;
2. HTN;
3. arteriosclerosis;
4. hyperlipidaemia;
5. pro-thrombotic conditions

Question 11

is the other eye at risk in CRVO

Answer 11

yes - the fellow eye may develop a retinal vein occlusion in 10% of people within 2-4yrs -> prevention by treating risk factors

Question 12

mild/non-ischaemic CRVO presentation

Answer 12

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/12-6/36

Question 13

will RAPD be +ve in mild CRVO

Answer 13

no -> maintained afferent visual input

Question 14

what changes occur to capillaries in CRVO and what does it lead to

Answer 14

damage to retinal capillary walls -> VEGF released -> leakage of plasma into the retina (macular oedema)

Question 15

macular oedema treatment

Answer 15

anti-VGEF intravitreal injection

Question 16

what does peripheral retinal ischaemia lead to (VGEF)

Answer 16

production of VGEF ->diffuses though the eye and stimulates growth of new blood vessels (rubeosis) on the iris and in the drainage angle -> can lead to angle closure glaucoma

Question 17

how can rubeosis be treated

Answer 17

panretinal photocoagulation (PRP) - destroys ischemic retina, minimizes the eye’s oxygen demand, and reduces the amount of VEGF being released

Question 18

branch retinal vein occlusion (BRVO) presentation

Answer 18

acute onset - often at night and noticed upon waking; PAINLESS loss of vision; visual acuity between 6/9-hand movementd at 1m

may be asymptomatic if fovea not affected

Question 19

BRVO retinal signs (4)

Answer 19

1. intraretinal haemorrhages in area of affected vein branch only;
2. engorged branch retinal vein;
3. macular oedema;
4. cotton wool spots

Question 20

is RAPD +ve in BRVO

Answer 20

no - smaller area of retina involved than CRVO

Question 21

BRVO complications (3)

Answer 21

macular oedema; retinal neovascularisation; vitreous haemorrhage

Question 22

what is hypertensive retinopathy

Answer 22

damage to the retina due to HTN

Question 23

what can lowgrade hypertensionlead to

Answer 23

accelerated ateriosclerosis

Question 24

retinal signs of hypertensive retinopathy (4)

Answer 24

thickened arteriole wall; “silver wiring” - increased central light reflex; narrowed/straightened arterioles; AV nipping - thickened arteriole constricts the venule

Question 25

what is geographical atrophy

Answer 25

chronic progressive degeneration of the macula - loss of patches of choroid/ retinal pigment epithelium/ retina in an irregular shape

Question 26

what is amaurosis fugax

Answer 26

"fleeting blindness" - transient and sudden monocular blindness (like a curtain coming down)

Question 27

what can cause amaurosis fugax (2)

Answer 27

1. carotid atheroma leading to emboli (fibrin-platelet/cholesterol); 2. cardiac valve emboli (calcific) - rarer

Question 28

what assessment must be done post amaurosis fugax

Answer 28

stroke risk assessment - TIA clinic for carotid scan, ECG, anti-platelet

Question 29

what is the life expectancy for pts w CRAO

Answer 29

5.5 years

Question 30

retinal presentation of CRAO (4)

Answer 30

1. pale retina/whitening - due to infarcted swollen inner 2/3 retina supplied by the CRA; 2. "cherry red spot" - fovea -> no inner retinal covering fovea centre and photorecptors supplied by choroidal circulation; 3. retinal artery narrowing; 4. emboli may be present; 5. boxcarring (segmental blood flow)

Question 31

4 causes of CRAO

Answer 31

1. carotic atheroma - 90% of CRAOs are embolic in nature; 2. calcified aortic valve lesions (emboli - rare); 3. GCA (must rule this out!); 4. traumatic vessel wall damage

Question 32

how can an embolus in the CRA attempt to be disloged

Answer 32

by lowering IOP -> aids the perfusion pressure gradient (usually ineffective)

Question 33

GCA symptoms (8)

Answer 33

1. headache; 2. temporal/scalp tenderness; 3. jaw claudication; 4. systemic symptoms (fever, lethargy malaise); 5. transient vision loss; 6. permanent ischaemic optic neuropathy; 7. retinal artery occlusion; 8. temproal artery thickening/tender/pulseless

Question 34

3 tests for GCA

Answer 34

1. BLOODS (raised ESR, CRP, platelets); 2. carotid ultrasound; 3. temporal atery biopsy

Question 35

is retinal artery occlusion an emergency?

Answer 35

yes - immediated systemic evaluation and referral to TIA service required

Question 36

what may patients who have CRAO concurrently present with

Answer 36

silent ischaemic stroke

Question 37

5 risk factors for retinal artery occlusive disease

Answer 37

1. older age (>70%); 2. diabetes mellitus; 3. arterial hypertension; 4. ischaemic heart disease; 5. smoking

Question 38

CRAO vs BRAO presentation

Answer 38

CRAO - Loss of vision over entire field; BRAO - hemi field defect (or may even have 6/6 vision if cilioretinal artery sparing)

Question 39

what vessels are usually involvedin BRAO

Answer 39

temporal retinal vessels

Question 40

BRAO treatment

Answer 40

does not usually require treatment unless perifoveolar vessels are threatened

Question 41

CRAO/BRAO investigations

Answer 41

1. FBC for anaemia, polycythemia, platelet disorders etc. ; 2. ESR/CRP for inflammatory ateritis; 3. fribrinogen levels, anti-APPL, aPTT, serum protein coagulopathies; 4. cholesterol, triglycerides, lipids for atherosclerotic disease; 5. echo/ECG for valve disease or AF; 6. blood cultures - bacterial endo/septic emboli

Question 42

2 managements fro RAO in emergency care

Answer 42

1. ocular massage - disloges the embolus to a point further down the arterial circulation and improves retinal perfusion; 2. anterior chamber paracentesis - if visual loss has been present <24hrs, slit-lamp removal of 0.1-0.4mL of aqueous humour to decrease IOP -> allows greater perfusion and embolus to be pushed further down the vascular tree

Question 43

medical therapy for CRAO

Answer 43

treatment is directed towards lowering IOP, increasinf retinal perfusion and increasing oxygen delivery to hypoxic tissues 1. timolol (start early); 2. acetazolamide + mannitol; 3. carbogen therapy (5%CO2, 95% O2) -> CO2 dilated retinal arterioles and O2 increases oxygen deliveryto ischaemic tissues; 4. hyperbaric oxygen therapy (if initiated within 2-12hrs)